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. Author manuscript; available in PMC: 2012 Oct 15.
Published in final edited form as: Biochem Pharmacol. 2011 May 14;82(8):915–930. doi: 10.1016/j.bcp.2011.05.001

Figure 2.

Figure 2

Structures of α7-active PAMs. The PAMs classified as type I, which increase the amplitude but do not strongly alter the kinetics of a7-mediated agonist evoked responses, are shown on the left. They include: CCMI, N-(4-chlorophenyl)-alpha-[[(4-chloro-phenyl)amino]methylene]-3-methyl-5-isoxazoleacet-amide; NS-1738, 1-(5-chloro-2-hydroxy-phenyl)-3-(2-chloro-5-trifluoromethyl-phenyl)-urea; Galantamine; 5-HI, 5-hydroxyindole; LY-2087101, [2-(4-fluoro-phenylamino)-4-methyl-thiazol-5-yl]-thiophen-3-yl-methanone; Genistein; and Ivermectin. Type II PAMs, which appear to slow or reverse α7 desensitization are shown on the right and include: PNU-120596, 1-(5-chloro-2,4-dimethoxy-phenyl)-3-(5-methyl-isoxazol-3-yl)-urea; TQS, 4-naphthalene-1-yl-3a,4,5,9b-tetrahydro-3-H-cyclopenta[c]quinoline-8-sulfonic acid amide; and A-867744, 4-(5-(4-chlorophenyl)-2-methyl-3-propionyl-1H-pyrrol-1-yl)benzenesulfonamide. PAMs proposed to be intermediate in their activity are shown in the center and include: JNJ-1930942, 2-[[4-fluoro-3-(trifluoromethyl)phenyl]amino]-4-(4-pyridinyl)-5-thiazolemethanol; and SB-206553, 3,5-dihydro-5-methyl-N-3-pyridinylbenzo [1,2-b:4,5-b′]-di pyrrole-1(2H)-carboxamide.